Pathology
Immune Responses
Type III hypersensitivity is mediated by which of the following:
Answer:
Type III hypersensitivity (immune complex-mediated hypersensitivity) occurs when antibodies (IgG) react to free soluble antigen by forming antibody-antigen complexes, called an immune complex. The immune complexes undergo opsonisation by complement and then are transported to the spleen where they are phagocytosed. If there is a rapid influx in antigen that overwhelms these mechanisms, then a type III hypersensitivity reaction occurs. Sites of predilection for the deposition of immune complexes include small blood vessels, kidneys and joints.Hypersensitivity Reactions
Pathology / Immune Responses
Last Updated: 13th April 2023
A group of diseases caused by an abnormal immune-mediated reaction. This may be directed as an exogenous antigen from the environment or a self-antigen.
Type I Hypersensitivity
Type I hypersensitivity (immediate hypersensitivity) is mediated by IgE, with immediate degranulation of mast cells and basophils. Overproduction of IgE in response to innocuous environmental antigen occurs in allergy and atopic individuals. Type I hypersensitivity reactions require an initial antigen exposure in order to sensitise the immune system, where lots of IgE is produced in response to that antigen. Mast cells have membrane receptors specific for the Fc portion of IgE, so that mast cells become coated in IgE. Subsequent exposure to the same antigen cross-linking mast cell surface IgE results in degranulation. Mast cells and basophils release their contents within minutes of exposure to an allergen (early phase response). The late phase response is mediated by eosinophils, responding to the same stimulus.
Examples of type I reactions include:
- Allergic rhinitis
- Allergic conjunctivitis
- Allergic asthma
- Systemic anaphylaxis
- Angioedema
- Urticaria
- Penicillin allergy
Type II Hypersensitivity
Type II hypersensitivity (antibody-mediated hypersensitivity) occurs when antibody (IgG or IgM) specific for cell surface antigens (either antibody to foreign cells or autoantibody) is produced. Cell destruction then occur via complement fixation, antibody-dependent cell-mediated cytotoxicity, and phagocytosis. Onset is normally rapid.
Examples of type II reactions include:
- Incompatible blood transfusions
- Haemolytic disease of the newborn
- Autoimmune haemolytic anaemias
- Goodpasture's syndrome
- Rheumatic heart disease
- Bullous pemphigoid
Type III Hypersensitivity
Type III hypersensitivity (immune complex-mediated hypersensitivity) occurs when antibodies (IgG) react to free soluble antigen by forming antibody-antigen complexes called an immune complex. The immune complexes undergo opsonisation by complement and then are transported to the spleen where they are phagocytosed. If there is a rapid influx in antigen that overwhelms these mechanisms, then a type III hypersensitivity reaction occurs. Sites of predilection for the deposition of immune complexes include small blood vessels, kidneys and joints.
Examples of type III reactions include:
- Extrinsic allergic alveolitis
- Systemic lupus erythematosus (SLE)
- Post-streptococcal glomerulonephritis
- Reactive arthritis
- Rheumatoid arthritis
Type IV Hypersensitivity
Type IV hypersensitivity (delayed T-cell-mediated hypersensitivity) is caused by activated T lymphocytes that injure cells by direct killing or releasing cytokines that activate macrophages. On first exposure to an antigen, a subset of T helper cells is activated and clonally expanded (this takes 1 - 2 weeks). On subsequent exposure to the same antigen, sensitised T helper cells secrete cytokines which attract and activate phagocytic macrophages. The type IV reactions peaks at 48 - 72 hours after contact with the antigen (time taken for recruitment and activation of macrophages). Type IV reactions are important for clearance of intracellular pathogens.
Examples of type IV reactions includes:
- Contact dermatitis
- Hashimoto's thyroiditis
- Primary biliary cholangitis
- Tuberculin skin test (Mantoux test)
- Chronic transplant rejection
- Granulomatous inflammation (e.g. sarcoidosis, Crohn's disease)
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
